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We aimed to evaluate the functions of long non-coding RNA taurine upregulated gene 1 (lncRNA TUG1) in renal ischemia-reperfusion (I/R) injury and identify the potential mechanisms. Pathological changes of renal tissues were examined using H&E staining after mimic renal I/R injury in vivo. The contents of serum renal functional parameters and inflammatory factors were measured. The expression of TUG1 and miR-449b-5p in renal tissues and HK-2 cells stimulated by I/R were detected. Then, the effects of TUG1 silencing on inflammation and apoptosis of cells were evaluated. Dual luciferase reporter assays were executed for determining the correlation between miR-449b-5p and TUG1, high mobility group box 1 (HMGB1), or matrix metalloproteinase 2 (MMP2). Subsequently, cells were co-transfected with miR-449b-5p mimic and pcDNA3.1 TUG1. The levels of inflammation, apoptosis, and the expression of HMGB1 and MMP2 were detected. The results revealed that renal tissues were obviously damaged after I/R accompanied by changes in renal functional markers and inflammatory factors. TUG1 was highly expressed whereas miR-449b-5p was lowly expressed. TUG1 silencing reduced the inflammation and apoptosis. Dual luciferase reporter assays confirmed that miR-449b-5p was a target of TUG1 as well as HMGB1 and MMP2 were direct targets of miR-449b-5p. Meanwhile, miR-449b-5p mimic presented the same results with TUG1 silencing, which were reversed after TUG1 overexpression. Moreover, MMP2 and HMGB1 expression was decreased after miR-449b-5p overexpression while that of was increased after TUG1 overexpression. These findings demonstrated that TUG1 silencing attenuates I/R-induced inflammation and apoptosis via targeting miR-449b-5p and regulating HMGB1 and MMP2 expression.
This article was published in the following journal.
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Providing summarized information on the clinical and biochemical characteristics and types of renal tubular acidosis in children in Assiut University Childern Hospital.
Patients presented with unexplained elevated serum creatinine including vast varieties of acute or chronic kidney disease. Renal biopsy may include acute and chronic interstitial nephritis...
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The prototypical uricosuric agent. It inhibits the renal excretion of organic anions and reduces tubular reabsorption of urate. Probenecid has also been used to treat patients with renal impairment, and, because it reduces the renal tubular excretion of other drugs, has been used as an adjunct to antibacterial therapy.
Inflammation of the interstitial tissue of the kidney. This term is generally used for primary inflammation of KIDNEY TUBULES and/or surrounding interstitium. For primary inflammation of glomerular interstitium, see GLOMERULONEPHRITIS. Infiltration of the inflammatory cells into the interstitial compartment results in EDEMA, increased spaces between the tubules, and tubular renal dysfunction.
A cytosolic carbonic anhydrase isoenzyme found widely distributed in cells of almost all tissues. Deficiencies of carbonic anhydrase II produce a syndrome characterized by OSTEOPETROSIS, renal tubular acidosis (ACIDOSIS, RENAL TUBULAR) and cerebral calcification. EC 4.2.1.-
A condition characterized by calcification of the renal tissue itself. It is usually seen in distal RENAL TUBULAR ACIDOSIS with calcium deposition in the DISTAL KIDNEY TUBULES and the surrounding interstitium. Nephrocalcinosis causes RENAL INSUFFICIENCY.
Bis(nitrato-O)dioxouranium. A compound used in photography and the porcelain industry. It causes severe renal insufficiency and renal tubular necrosis in mammals and is an effective lymphocyte mitogen.
Nephrology - kidney function
Nephrology is a specialty of medicine and pediatrics that concerns itself with the study of normal kidney function, kidney problems, the treatment of kidney problems and renal replacement therapy (dialysis and kidney transplantation). Systemic conditions...